解剖学报 ›› 2014, Vol. ›› Issue (2): 239-241.doi: 10.3969/j.issn.0529-1356.2014.02.017

• 肿瘤生物学 • 上一篇    下一篇

Notch信号通路在血小板衍生生长因子-BB诱导人胰腺癌细胞增殖过程中的作用

马永超 范文娟 吴华 王福清*   

  1. 漯河医学高等专科学校基础医学部生物化学与分子生物学教研室,河南 漯河 462002
  • 收稿日期:2013-09-10 修回日期:2013-11-17 出版日期:2014-04-06 发布日期:2014-04-06
  • 通讯作者: 王福清 E-mail:wfq22000@yahoo.com.cn
  • 基金资助:

    诱导多能干细胞促小脑平行纤维损伤后再生及其突触重建的实验性研究

Role of Notch signaling in platelet derived growth factor-BB induced proliferation of human pancreatic adenocarcinoma

MA Yong-chao FAN Wen-juan WU Hua WANG Fu-qing*   

  1. Department of Biochemistry and Molecular Biology, Basic Medical Institute, Luohe Medical College, He’nan  Luohe 46200, China
  • Received:2013-09-10 Revised:2013-11-17 Online:2014-04-06 Published:2014-04-06
  • Contact: WANG Fu-qing E-mail:wfq22000@yahoo.com.cn

摘要:

目的 探讨Notch信号通路在血小板衍生生长因子(PDGF)-BB诱导人胰腺癌细胞(HPAC)增殖过程中的作用。 方法 MTT法检测PDGF-BB及γ-secretase 抑制剂4’,6-二脒基-2-苯基吲哚(DAPT)对HPAC增殖活力的影响;Western blotting检测细胞Notch蛋白表达水平的变化;染色质免疫共沉淀(CHIP)检测Notch下游靶基因转录水平的变化。 结果 PDGF-BB显著促进HPAC增殖,提高细胞Notch表达水平,增强Notch靶基因的转录;不同剂量的DAPT及血小板衍生生长因子受体(PDGFR)抑制剂处理细胞,显著反转了PDGF-BB的作用。结论 Notch信号通路在PDGF-BB诱导胰腺癌细胞增殖中起到重要作用。

Abstract:

Objective To clarify Notch signaling in platelet derived growth factor-BB(PDGF-BB) induced proliferation of human pancreatic adenocarcinoma (HPAC). Methods After being treated by PDGF-BB and (or) γ-secretase inhibitor DAPT, changes of HPAC cell proliferation were detected by MTT assay; Alterations of Notch level in HPAC cells were measured by Western blotting assay; Variations of capability in cardiolipin synthetic lecithin(CSL) binding to the promoter of target gene hes-1 were identified by chromatin immunoprecipitation (CHIP) assay. Results PDGF-BB facilitates the proliferation of HPAC cells, upregulates Notch level and enhances the capability in CSL binding to the promoter of hes-1. DAPT and PDGFR inhibitor treatment suppresses and invalidates PDGF-BB effection. Conclusion Notch-1 signaling plays an essential role in the modulation of PDGF-BB-induced proliferation of HPAC cells.